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Review
. 2016 Aug 21;22(31):7030-45.
doi: 10.3748/wjg.v22.i31.7030.

Hepatitis E: Discovery, global impact, control and cure

Mohammad S Khuroo  1 , Mehnaaz S Khuroo  1 , Naira S Khuroo  1
Affiliations
Review

Hepatitis E: Discovery, global impact, control and cure

Mohammad S Khuroo et al. World J Gastroenterol. .

Abstract

Hepatitis E was identified as an epidemic of non-A, non-B hepatitis from Kashmir, India in 1978. Hepatitis E virus (HEV), the etiological agent is the sole member of family Hepeviridae. The virus has marked heterogeneity and infects many animals like bats, camel, chicken, deer, boar, mongoose, pigs, rats, rabbit and cutthroat trout. Hepatitis E is a disease with a major global impact and has two distinct epidemiological patterns. Hepatitis E is an imperative health issue in developing nations, transmitted through sullied water and happens most every now in young adults. The disease is particularly severe during pregnancy and in people with underlying liver cirrhosis. Autochthonous hepatitis E is increasingly recognized in developed countries. The virus infects domestic pigs, wild boar and Sika deer in these countries. HEV infections in humans occur by eating the undercooked game flesh, raw liver from supermarkets and Figatelli sausages. Blood transfusion-associated HEV infections occur in many countries and screening of donors for HEV RNA is under consideration. Hepatitis E causes a number of extrahepatic diseases, including a wide spectrum of neurological syndromes. HEV genotype 3 causes prolonged viremia, chronic hepatitis, liver fibrosis and cirrhosis in organ transplant patients. The virus is amenable to ribavirin monotherapy and most patients clear the virus in a few weeks. Hepatitis E vaccine -239, marketed in China, has shown high efficacy with sustained protection for over four years.

Keywords: Communicable diseases; Discovery; Hepatitis E; Hepatitis E virus; Vaccine; Zoonosis.

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Figures

Figure 1
Figure 1
Hepatitis E virus. Genomic organization. A: The hepatitis E virus genome; B: Genomic RNA and bicistronic subgenomic RNA; C: Open reading frames (ORFs) and (D) 3 encoded proteins (pORF1, pORF2 and pORF3). For details, see text about hepatitis E virus. Adopted from Khuroo et al[143], 2016.
Figure 2
Figure 2
Proposed replication of hepatitis E virus. For details, see text about hepatitis E replication. Adopted from Khuroo et al[143], 2016.
Figure 3
Figure 3
Evolutionary history of hepatitis E virus. The times to the most recent common ancestors (tMRCAs) for all four genotypes of HEV were calculated using BEAST to conduct a Bayesian analysis of HEV. The population dynamics for genotypes 1, 3 and 4 were analyzed using skyline plots. For details see text on HEV evolution. Source of data Purdy et al[50] 2010. HEV: Hepatitis E virus.
Figure 4
Figure 4
Global distribution of hepatitis E disease. See text under “global distribution” for explanation.
Figure 5
Figure 5
Global distribution of hepatitis E virus genotypes. See text under “global distribution” for explanation.
See this image and copyright information in PMC

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